Synaptic plasticity and depression: New insights from stress and rapid-acting antidepressants
By R. Duman, G. Aghajanian, G. Sanacora, John H. Krystal. Nature Medicine, 2016
1,559 citations recorded by the source corpus.
Depression is a common, devastating illness. Current pharmacotherapies help many patients, but high rates of a partial response or no response, and the delayed onset of the effects of antidepressant therapies, leave many patients inadequately treated. However, new insights into the neurobiology of stress and human mood disorders have shed light on mechanisms underlying the vulnerability of individuals to depression and have pointed to novel antidepressants. Environmental events and other risk factors contribute to depression through converging molecular and cellular mechanisms that disrupt neuronal function and morphology, resulting in dysfunction of the circuitry that is essential for mood regulation and cognitive function. Although current antidepressants, such as serotonin-reuptake inhibitors, produce subtle changes that take effect in weeks or months, it has recently been shown that treatment with new agents results in an improvement in mood ratings within hours of dosing patients who are resistant to typical antidepressants. Within a similar time scale, these new agents have also been shown to reverse the synaptic deficits caused by stress.
Subfields: Biological Psychiatry, Cellular and Molecular Neuroscience, Pharmacology
View Paper: https://www.semanticscholar.org/paper/cb1fcffcccbd09f3e331fe7d8e63de0c3285a0c1
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Citations in the corpus
- The Link between Depression and Chronic Pain: Neural Mechanisms in the Brain (2017, background): “BDNF belongs to the family of neurotrophic factors and is not only involved in the signaling pathways of the PFC and hippocampal dentate gyrus together with its receptor tropomyosin receptor kinase B (TrkB) but is also important in regulating neuroplasticity [32, 33].”
- Psychedelics Promote Structural and Functional Neural Plasticity (2018, background): “A preponderance of evidence from a combination of human imaging, postmortem studies, and animal models suggests that atrophy of neurons in the prefrontal cortex (PFC) plays a key role in the pathophysiology of depression and related disorders and is precipitated and/or exacerbated by stress (Arnsten”
- TSception: Capturing Temporal Dynamics and Spatial Asymmetry From EEG for Emotion Recognition (2021, background): “…plays an important role in Cognitive Behavioural Therapy (CBT) [3], Emotion Regulation Therapy (ERT)/Emotion-Focused Therapy (EFT) [4], [5], [6], and the evaluation of medical treatment [7] for emotion-related mental disorders, such as Generalized Anxiety Disorder (GAD) [8], and Depression [9].”
- Altered connectivity in depression: GABA and glutamate neurotransmitter deficits and reversal by novel treatments (2019, background): “Preclinical studies in rodents and nonhuman primates have reported structural alterations in chronic stress models, including atrophy of neurons in the hippocampus and prefrontal cortex (PFC) (Duman et al., 2016; McEwen et al., 2015; McEwen and Morrison, 2013).”